PMID- 1682217
OWN - NLM
STAT- MEDLINE
DCOM- 19911216
LR  - 20190516
IS  - 0890-9369 (Print)
IS  - 0890-9369 (Linking)
VI  - 5
IP  - 11
DP  - 1991 Nov
TI  - v-erbA overexpression is required to extinguish c-erbA function in erythroid cell 
      differentiation and regulation of the erbA target gene CAII.
PG  - 2033-47
AB  - The v-erbA oncoprotein represents a retrovirus-transduced oncogenic version of 
      the thyroid hormone (T3/T4) receptor c-erbA (type alpha). It contributes to 
      virus-induced erythroleukemia by efficiently arresting differentiation of red 
      cell progenitors and by suppressing transcription of erythrocyte-specific genes. 
      Here, we show that v-erbA and c-erbA bind directly to sequences within the 
      promoter of the erythrocyte-specific carbonic anhydrase II (CAII), a gene whose 
      transcription is efficiently suppressed by v-erbA. This erbA-binding site confers 
      thyroid hormone responsiveness to a heterologous promoter in transient expression 
      experiments and is a target for efficient down-regulation of CAII transcription 
      by the v-erbA oncoprotein. In stably transformed erythroblasts coexpressing the 
      v-erbA oncoprotein and the c-erbA/T3 receptor at an approximately equimolar 
      ratio, c-erbA activity is dominant over v-erbA. T3 efficiently induced erythroid 
      differentiation in these cells, thus overcoming the v-erbA-mediated 
      differentiation arrest. Likewise, T3 activated CAII transcription as well as 
      transient expression of a T3-responsive reporter gene containing the 
      CAII-specific erbA-binding site. The c-erbA-dependent activation of this CAII 
      reporter construct could only be suppressed by very high amounts of v-erbA. Our 
      results suggest that overexpression of v-erbA is required for its function as an 
      oncoprotein.
FAU - Disela, C
AU  - Disela C
AD  - Institute for Molecular Pathology, Wien, Austria.
FAU - Glineur, C
AU  - Glineur C
FAU - Bugge, T
AU  - Bugge T
FAU - Sap, J
AU  - Sap J
FAU - Stengl, G
AU  - Stengl G
FAU - Dodgson, J
AU  - Dodgson J
FAU - Stunnenberg, H
AU  - Stunnenberg H
FAU - Beug, H
AU  - Beug H
FAU - Zenke, M
AU  - Zenke M
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Genes Dev
JT  - Genes & development
JID - 8711660
RN  - 0 (Oncogene Proteins v-erbA)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Receptors, Thyroid Hormone)
RN  - 0 (Retroviridae Proteins, Oncogenic)
RN  - 06LU7C9H1V (Triiodothyronine)
RN  - EC 1.13.12.- (Luciferases)
RN  - EC 4.2.1.1 (Carbonic Anhydrases)
RN  - I16QD7X297 (Neomycin)
SB  - IM
GS  - CAII
MH  - Base Sequence
MH  - Binding Sites/genetics
MH  - Blotting, Northern
MH  - Carbonic Anhydrases/*genetics
MH  - Cell Differentiation/drug effects/*genetics
MH  - Cell Line, Transformed
MH  - Drug Resistance/genetics
MH  - Erythroblasts/*cytology/drug effects/metabolism
MH  - Gene Expression Regulation/*genetics
MH  - Genes, gag/genetics
MH  - HeLa Cells
MH  - Humans
MH  - Luciferases/genetics
MH  - Molecular Sequence Data
MH  - Neomycin/pharmacology
MH  - Oncogene Proteins v-erbA
MH  - Plasmids/genetics
MH  - Precipitin Tests
MH  - Proto-Oncogene Proteins/*genetics
MH  - Receptors, Thyroid Hormone/genetics
MH  - Retroviridae Proteins, Oncogenic/*genetics
MH  - Triiodothyronine/pharmacology
MH  - Vaccinia virus/genetics
EDAT- 1991/11/01 00:00
MHDA- 1991/11/01 00:01
CRDT- 1991/11/01 00:00
PHST- 1991/11/01 00:00 [pubmed]
PHST- 1991/11/01 00:01 [medline]
PHST- 1991/11/01 00:00 [entrez]
AID - 10.1101/gad.5.11.2033 [doi]
PST - ppublish
SO  - Genes Dev. 1991 Nov;5(11):2033-47. doi: 10.1101/gad.5.11.2033.